Acut kidney injury Flashcards Preview

Nephrology > Acut kidney injury > Flashcards

Flashcards in Acut kidney injury Deck (50)
Loading flashcards...

What are the usual causes of acute interstitial nephritis? Presentation? Lab abnormalities?

- most cases related to med use
- also caused by bacterial, viral or fungal infections of the kidney
presentation- 1/3 of time hx of maculopapular rash, fever, and arthralgias
labs- EOSINOPHILS in urine


What is the most common type of acute intrinsic renal injury? 3 main causes?

- 3 main causes:
ischemia, sepsis, and nephrotoxic drugs


When does ATN occur?

- when tubules fail to fxn
- failure to reabsorb BUN so BUN/Cr ratio should be less than 10:1
- failure to reabsorb Na and water = lead to elevated urine Na+ (greater than 20) and low urine SG and osmolality (less than 450)
- cell sloughing causes urine to be positive for sediment = MUDDY BROWN casts (granular), renal tubular epithelial cells and epithelial cell casts


Why would ATN be secondary to ischemia?

- tubular damage from site of low perfusion
- inadequate GFR (prerenal) but also by decreased renal blood flow to renal cellular fxnl units due to:
prolonged hypotension
prolonged surgery (esp cardiac and major vascular)


How can ATN be secondary to toxins?

- may occur 5-10 days after exposure
- aminoglycosides (up to 25% of pts receiving thes drugs):
gentamicin, amikacin (Most nephrotoxic), streptomycin and tobramycin
- amphotericin B
- chemo
- acyclovir
- ethlyene glycol (anti-freeze)
- sulfonamides, cephalosporins


What is contrast nephropathy?

- form of ATN
- occurs 24-48 hrs post contrast exposure
- risk factors for development: DM, CKD, high contrast load, concurrent use of nephrotoxic drugs, age
- mechanism of injury unclear but likely involves:
direct toxicity of reactive O2 species (free radicals)
contrast induced diuresis
increased urinary viscosity
increased O2 consumption
imbalance of vasoconstriction vs vasodilation


How can we prevent contrast nephropathy?

- min amt of contrast used - talk to radiologist
- hydrate pre and post procedure with NS
- mucomyst (N-Acetylcysteine): 600 mg po BIDx 3 days starting day prior to procedure
- stop metformin (glucophage) the day of contrast load and for 48 hr post (can lead to lactic acidosis)
- Ask yourself: Do you really need this test? any alternatives?


Other causes of ATN?

- blood transfusion rxn, hemolytic anemia
- multiple myeloma
- uric acid
- myoglobin: muscle breakdown, when severe called rhabdomyolysis (CK greater than 16000), crush injuries, muscle necrosis from pressure pts in unconscious pts, seizures, cocaine, and ETOH


What is the FENa used for?

- useful for determining if the casue of AKI is prerenal or ATN
- prerenal if FENa is less than 1%
- intrinsic if FENa is greater than 2%


What are dark granular and epithelial casts indicators of?

- pure ATN


What are crystals an indicator of?

- crystalluric ARF


What are WBCs and WBC casts indicators of?

- acute interstitial nephritis


What are RBCs and RBC casts indicators of?

- proliferative/necrotizing glomerulonephritis


Management of AKI?

- tx underlying cause!!!
- maintain euvolemia
- manage electrolytes
- manage BP
- stop potentially nephrotoxic meds!!!!
- may need temporally dialysis


General work up of AKI?

- assess volume status
- UA: dipstick, microscopic exam, urine Na+, urine Cr
- serum BUN and Creatinine (BMP)
- fractional excretion of NA+


What imaging studies do you want to do in intrinsic AKI?

- renal US
- bladder scan for post void residual
- CT or MRI
- renal bx in certain cases


What test is most impt noninvasive test in dx eval of pts with AKI?

- UA


Labs of prerenal AKI?

- urine Na is going to be less than 20
- BUN/Cr ratio will be more than 20:1
- FEna is less than 1


Labs of intrinsic AKI?

- Urine Na will be greater than 20
- BUN/Cr ratio less than 10:1, and FEna is greater than 2


Labs of postrenal AKI?

- urine Na will vary
- BUN/Cr will be nomral 10-20:1
- FEna will be variable